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Action of the neurotoxin β‐ N ‐oxalyl‐L‐α,β‐diaminopropionic acid on glutamate metabolism of brain mitochondria
Author(s) -
Duque-Magalhaes M.C.,
Packer Lester
Publication year - 1972
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(72)80337-5
Subject(s) - chemistry , philosophy
Mammalian neurolathyrism is a progressive and degenerative disease of central nervous system originating from excessive consumption of Lafhyrus seeds, particularly those of L. sativus. Rao et al. [I] have isolated P-N-oxalyl-L-a&diaminopropionic acid (ODAP) from the seeds of L. satiuus and shown this substance to be the neurotoxin [ 1, 21 Characterization of the biochemical effect and cellular site of action of ODAP is required for clarifying the relation between chronic ingestion of this substance, its neurotoxicity, and degenerative effects in the brain. ODAP is structurally analogous to glutamate. Since glutamate and ammonia metabolism are associated with mitochondria, and because acute doses of ODAP led to ammonia toxicity in rats [3], an investigation of the action of ODAP on glutamate metabolism in isolated brain mitochondria was undertaken. The results presented in this communication show brain a)